a. Field of the Invention
This invention relates to diabetes treatment and is more particularly concerned with diabetes mellitus. The present invention is considered to be suitable for the treatment of either type I (insulin-dependent) or type II (non-insulin-dependent) diabetes mellitus.
b. Description of the Related Art
It has been observed by R. L. Reid et al (".beta.-endorphin stimulates the secretion of Insulin and Glucagon in Diabetes Mellitus", Metabolism, Vol 33, No 3 (March), 1984, pages 197-199) that administration of human .beta.-endorphin (2.5 mg by intravenous bolus injection) to three subjects with non-insulin dependent diabetes mellitus (type II) induced prompt and simultaneous increments in the plasma concentrations of insulin and glucagon lasting up to 90 minutes and that, in contrast to the hyperglycemic response previously observed in normal subjects following administration of .beta.-endorphin, these diabetics showed a progressive decline in plasma glucose throughout a three hour study period. However, this progressive decline in plasma glucose was substantially unaffected by the administration of .beta.-endorphin which took place one hour after the start of the study period.
It has been observed by the inventor that, in normal mice, there are only a small number of .beta.-endorphin receptors on the muscle fibres, whereas in obese (ob/ob) diabetic mice, there is a dramatically higher density of .beta.-endorphin receptors on the muscles. The obese (ob/ob) mice inherit diabetes mellitus which resembles type II (non-insulin-dependent) diabetes mellitus seen in humans. In both the human and the mouse with this condition, the muscles are insulin-resistant. The present invention is based on the surprising discovery that blood glucose levels can be reduced by administration of .beta.-endorphin fragments which do not include the opioid (N-terminal) region of .beta.-endorphin, and that such fragments act by enhancing the uptake of glucose into the muscle by a non-insulin dependent route .